Subwavelength localization and toroidal dipole moment of spoof surface plasmon polaritons

We experimentally and theoretically demonstrate subwavelength scale localization of spoof surface plasmon polaritons at a point defect in a two-dimensional groove metal array. An analytical expression for dispersion relation of spoof surface plasmon polaritons substantiates the existence of a band gap where a defect mode can be introduced. A waveguide coupling method allows us to excite localized spoof surface plasmon polariton modes and measure their resonance frequencies. Numerical calculations confirm that localized modes can have a very small modal volume and a high Q factor both of which are essential in enhancing light-matter interactions. Interestingly, we find that the localized spoof surface plasmon polariton has a significant toroidal dipole moment, which is responsible for the high Q factor, as well as an electric quadrupole moment. In addition, the dispersion properties of spoof surface plasmon polaritons are analyzed using a modal expansion method and numerical calculations

Driving in ZZ Ceti stars - Problem solved?

There is a fairly tight correlation between the pulsation periods and effective temperatures of ZZ Ceti stars (cooler stars have longer periods). This seems to fit the theoretical picture, where driving occurs in the partial ionization zone, which lies deeper and deeper within the star as it cools. It is reasonable to assume that the pulsation periods should be related to the thermal timescale in the region where driving occurs. As that region sinks further down below the surface, that thermal timescale increases. Assuming this connection, the pulsation periods could provide an additional way to determine effective temperatures, independent of spectroscopy. We explore this idea and find that in practice, things are not so simple.Comment: 4 pages, 3 figure

Search for supersolidity in 4He in low-frequency sound experiments

We present results of the search for supersolid 4He using low-frequency, low-level mechanical excitation of a solid sample grown and cooled at fixed volume. We have observed low frequency non-linear resonances that constitute anomalous features. These features, which appear below about 0.8 K, are absent in 3He. The frequency, the amplitude at which the nonlinearity sets in, and the upper temperature limit of existence of these resonances depend markedly on the sample history.Comment: Submitted to the Quantum Fluids and Solids Conf. Aug. 2006 Kyot

Annealing Effect for Supersolid Fraction in 4^4He

We report on experimental confirmation of the non-classical rotational inertia (NCRI) in solid helium samples originally reported by Kim and Chan. The onset of NCRI was observed at temperatures below ~400 mK. The ac velocity for initiation of the NCRI suppression is estimated to be ~10 $\mu$m/sec. After an additional annealing of the sample at $T= 1.8$ K for 12 hours, ~ 10% relative increase of NCRI fraction was observed. Then after repeated annealing with the same conditions, the NCRI fraction was saturated. It differs from Reppy's observation on a low pressure solid sample.Comment: to be published in J. of Low Temp. Phys. (QFS2006 proceedings

Functional rescue of dystrophin deficiency in mice caused by frameshift mutations using Campylobacter jejuni Cas9

Duchenne muscular dystrophy (DMD) is a fatal, X-linked muscle wasting disease caused by mutations in the DMD gene. In 51% of DMD cases, a reading frame is disrupted because of deletion of several exons. Here, we show that CjCas9 derived from Campylobacter jejuni can be used as a gene editing tool to correct an out-of-frame Dmd exon in Dmd knockout mice. Herein, we used Cas9 derived from S. pyogenes to generate Dmd knockout (KO) mice with a frameshift mutation in Dmd gene. Then, we expressed CjCas9, its single-guide RNA, and the eGFP gene in the tibialis anterior muscle of the Dmd KO mice using an all-in-one adeno-associated virus (AAV) vector. CjCas9 cleaved the target site in the Dmd gene efficiently in vivo and induced small insertions or deletions at the target site. This treatment resulted in conversion of the disrupted Dmd reading frame from out-of-frame to in-frame, leading to the expression of dystrophin in the sarcolemma. Importantly, muscle strength was enhanced in the CjCas9-treated muscles, without off-target mutations, indicating high efficiency and specificity of CjCas9. This work suggests that in vivo DMD frame correction, mediated by CjCas9 has great potential for the treatment of DMD and other neuromuscular diseases

Cadherin composition and multicellular aggregate invasion in organotypic models of epithelial ovarian cancer intraperitoneal metastasis.

During epithelial ovarian cancer (EOC) progression, intraperitoneally disseminating tumor cells and multicellular aggregates (MCAs) present in ascites fluid adhere to the peritoneum and induce retraction of the peritoneal mesothelial monolayer prior to invasion of the collagen-rich submesothelial matrix and proliferation into macro-metastases. Clinical studies have shown heterogeneity among EOC metastatic units with respect to cadherin expression profiles and invasive behavior; however, the impact of distinct cadherin profiles on peritoneal anchoring of metastatic lesions remains poorly understood. In the current study, we demonstrate that metastasis-associated behaviors of ovarian cancer cells and MCAs are influenced by cellular cadherin composition. Our results show that mesenchymal N-cadherin-expressing (Ncad+) cells and MCAs invade much more efficiently than E-cadherin-expressing (Ecad+) cells. Ncad+ MCAs exhibit rapid lateral dispersal prior to penetration of three-dimensional collagen matrices. When seeded as individual cells, lateral migration and cell-cell junction formation precede matrix invasion. Neutralizing the Ncad extracellular domain with the monoclonal antibody GC-4 suppresses lateral dispersal and cell penetration of collagen gels. In contrast, use of a broad-spectrum matrix metalloproteinase (MMP) inhibitor (GM6001) to block endogenous membrane type 1 matrix metalloproteinase (MT1-MMP) activity does not fully inhibit cell invasion. Using intact tissue explants, Ncad+ MCAs were also shown to efficiently rupture peritoneal mesothelial cells, exposing the submesothelial collagen matrix. Acquisition of Ncad by Ecad+ cells increased mesothelial clearance activity but was not sufficient to induce matrix invasion. Furthermore, co-culture of Ncad+ with Ecad+ cells did not promote a 'leader-follower' mode of collective cell invasion, demonstrating that matrix remodeling and creation of invasive micro-tracks are not sufficient for cell penetration of collagen matrices in the absence of Ncad. Collectively, our data emphasize the role of Ncad in intraperitoneal seeding of EOC and provide the rationale for future studies targeting Ncad in preclinical models of EOC metastasis